**1. Introduction**

Whitefly, *B. tabaci* (Gennadius, 1889) (Hemiptera: Aleyrodidae) is a pest of global significance. It is a serious pest of vegetable, field, and ornamental crops [1–3]. This notorious pest shares global distribution as an important pest in field as well as in greenhouse production systems [2, 4]. Both the nymph and adult cause severe economic loss to the growers by direct sucking sap from the phloem and thereby reducing the yield. They also cause indirect damage by transmitting the virus [5] and excreting honeydew on leaves. As a result of honeydew secretion, black sooty mold develops that impairs photosynthesis ability of the infested plants. *B. tabaci* is considered as complex of biotypes [4, 6, 7] and composed of at least 40 morphologically indistinguishable species [8–11]. These biotypes/species are mainly differentiated based on biochemical or molecular polymorphism markers. There are mainly two types of biotypes *viz.,* biotype B and biotype Q. Biotype B is considered to be originated from the Middle East–Asia Minor region (Middle East Asia Minor 1 —MEAM1 group) [9] whereas biotype Q possibly originated in the Iberian Peninsula Mediterranean—MED group) [12, 13].

The various biotype of this tiny fly causes significant economic loss. Henneberry and Faust [14] reported approximately 10 billion US dollars (USD) economic loss

during the years 1980 to 2000 due to whitefly infestation. They also revealed that there were about 300 USD economic losses due to the infestation of whitefly in different bean crops during 1991. Cotton growers in Arizona, California, and Texas spent 154 million USD during 1994–1998 to control the whitefly [15]. This pest is listed as one of the top 100 invasive species of the world by IUCN. Due to the severity of infestation and polyphagous in nature, farmers largely depend on the chemical management of this pest. As a result of the extensive application of synthetic insecticides, *B. tabaci* has developed multifold resistance to a wide range of insecticides.

#### **2. Insecticide resistance in** *B. tabaci*

Insecticide resistance is one of the important threats in the changing agricultural scenario. It has been increasing at an alarming rate since the introduction of synthetic insecticides. The first case of insecticide resistance was documented by A.L. Melander in 1914. He reported that the San Jose scale was resistant to lime sulfur. Since then many pests have developed various degrees of resistance against various insecticides. The list is ever-growing.

In Turkey, the whitefly population (Biotype B) showed 20–310-fold resistance to OPs [16]. In India, Asia 1 whiteflies showed high resistance to OPs such as acephate and triazophos [17]. The population from China showed a low level of resistance to chlorpyriphos, dichlorvos, and carbosulfan (carbamate) [18, 19].

This pest has also developed various degrees of resistance against synthetic pyrethroids and neonicotinoids. The magnitude of resistance varies from region to region, and it mainly depends on the frequency of insecticide use. B biotype population from northwestern China [20] and Cyprus [21] showed very high resistance against cypermethrin and bifenthrin. Neonicotinoids were introduced as one of the most important chemicals against whitefly and they also performed well due to their systemic and translaminar properties and high residual activity [22–24]. However, due to their frequent and extensive use, resistance against these chemicals has been reported from different corners of the world. The first report of neonicotinoid resistance was published in 1996, describing the low efficacy of imidacloprid against *B. tabaci* [25]. Low-to-moderate levels of resistance to imidacloprid and thiamethoxam were reported from Brazil [26], whereas high levels of resistance were detected from Florida [27]. The same biotype of the pest showed different degrees of resistance to the same class of insecticide. Biotype Q in Israel showed a high level of resistance to thiamethoxam but a moderate level of resistance against imidacloprid and acetamiprid [28]. Control failure of whitefly with neonicotinoid has been reported from Pakistan also. It is due to neonicotinoid resistance in *B. tabaci* [29]. Naveen et al. [30] reported a high degree of resistance against neonicotinoids from India (Asia I and Asia II-1). Neonicotinoid resistance has also been reported from different parts of China both in biotype B and Q [18, 19, 31]. Biotype Q population of southeastern Spain showed 1–7-fold resistance (low level) against spiromesifen [32] whereas 8–32-fold resistance has been reported from India [17]. Astonishingly, several field populations from Spain showed more than 10,000-fold resistance against spiromesifen [33]. Insect growth regulators (pyriproxyfen and buprofezin) are also proving vulnerable to resistance by *B. tabaci* [17, 34–36]. These two chemicals, that is, pyriproxyfen and buprofezin act primarily against immature stages of whiteflies. They have distinct modes of action. Therefore, the chance of cross-resistance is very low. Buprofezin is a chitin synthesis inhibitor and results in nymphal death during ecdysis [37], whereas pyriproxyfen is a juvenile hormone mimic inter-rupting nymphal and pupal

*Insecticide Resistance in Whiteflies* Bemisia tabaci *(Gennadius): Current Global Status DOI: http://dx.doi.org/10.5772/intechopen.101954*

#### **Figure 1.** *A general pathway for insecticide detoxification.*

development. It also suppresses egg hatching by direct exposure of eggs or transovarially *via* the treatment of adult females [38]. Resistance to buprofezin was first detected in the Netherlands and thereafter from Spain and Israel [39, 40]. Commercial introduction of pyriproxyfen for management of whitefly was done in the year 1991 in Israel. Within 1 year of its introduction, whitefly developed about 550-fold resistance at LC50 and it was reported from a rose greenhouse that had previously been sprayed only three times with this chemical [40, 41].

Resistance in *B. tabaci* is known to be multi-factorial based on multiple mechanisms. Enhanced detoxification and modifications to acteyl-cholinesterase (AChE), GABA-gated chloride-ion channel, and voltage-sensitive sodium channel are important mechanisms. Pesticide detoxifying enzymes play an important role in reducing the susceptibility of insecticides. Insecticides are generally hydrophobic in nature. Metabolism converts water-insoluble (apolar) or fat-soluble (lipophilic) insecticides into polar compounds or less lipophilic compounds. Conversion of apolar substances to less lipophilic or polar metabolites takes place by two reactions, that is, phase I (primary) and phase II (secondary) reactions. The phase I metabolites are sometimes polar enough to be excreted but are usually further converted to water-soluble conjugates by phase II reactions. A general insecticide detoxification pathway is as follows (**Figure 1**).
